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NMSP Exam II > [PATH] Bones, Joints and Soft Tissue (Part 1 BONE) [Martin] > Flashcards

[PATH] Bones, Joints and Soft Tissue (Part 1 BONE) [Martin] Flashcards

1
Q

This image depicts what type of process?

A

Endochondral ossification

(in a calcaneus)

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2
Q

Root word association:

Osteoporosis =

Osteomalacia =

Osteopetrosis =

Osteogenesis imperfecta =

Osteitis deformans =

Osteodystrophy =

A

Osteoporosis = Porous; thinned out bone

Osteomalacia = Weakened, soft bone

Osteopetrosis = Peter=rock, stone bone

Osteogenesis imperfecta = Imperfect origin of bone

Osteitis deformans = Deforming bone-itis

Osteodystrophy = Difficult/bad growing bone

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3
Q

What are the (2) components of bone matrix?

A

Osteoid

Mineral component

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4
Q

Hardness of bones is due to?

A

Hydroxyapatite

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5
Q

What are the components of osteoid?

A

Type I collagen with small amounts of glycosaminoglycans and other proteins

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6
Q

What is the protein found in osteoid?

Produced by what?

Function?

How can you utilize osteopontin levels?

A

Osteopontin (aka osteocalcin)

  • produced by osteoblasts
  • function: contributes to the regulation of bone formation, mineralization, and calcium homeostasis
  • utilization: serum osteopontin levels are used as a sensitive and specific marker of osteoblast activity
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7
Q

What are the (2) histologic forms of bone?

A

Woven

Lamellar

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8
Q

Characteristics of woven bone?

A
  • Disorganized
  • Haphazard arrangement of collagen= less structural integrity
  • Produced rapidly ; fetal development and fracture repair
  • Abnormal in adults, but not specific for any bone disease
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9
Q

Characteristics of lamellar bone?

A

Slow production

Parallel collagen

Strong

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10
Q

Function of osteoblasts

A

Synthesize, transport and assemble matrix

*Regulates mineralization

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11
Q

Function of osteocytes?

A

-Inactive osteoblasts (inactive osteoblasts can be recognized by a decrease in cytoplasmic volume)

  • Control calcium and phosphate levels
  • detect mechanical forces and translate them into biological activity in a process known as mechanotransduction
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12
Q

How are osteocytes interconnected?

A

by an intricate network of dendritic cytoplasmic processes through tunnels (canaliculi)

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13
Q

What are osteoclasts?

Function?

A

Multinucleated macrophages derived from circulating monocytes

Bone resorption

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14
Q

What is a resorption pit?

A

When surface integrin proteins allow osteoclasts to attach to the matrix and create a sealed extracellular trench (a resorption pit)

-Secretion of acid and neutral proteases, predominantly matrix metalloproteases (MMPs), into the pit results in dissolution of inorganic and organic components of bone

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15
Q

What type of bone is associated with:

Endochondral ossification?

Intramembranous ossification?

A

Endochondral ossification = Long bones

Intramembranous ossification = Flat bones

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16
Q

What is the name for the cartilage mold that bones develop from during endochondral ossification?

A

anlagen

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17
Q

A central medullary canal within the anlagen is created by what in the process of endochondral ossification?

A

chondroblasts

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18
Q

In the process of endochondral ossification, where do osteoblasts begin to deposit the cortex?

A

beneath the periosteum of the diaphysis (midshaft)

-this forms a primary center of ossification resulting in radial growth

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19
Q

During endochondral ossification, where is new bone deposited?

A
  • new bone is deposited at the bottom of growth plates (epiphyses)
  • this leads to longitudinal growth (secondary centers of ossification)
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20
Q

What is the general process of intramembranous ossification? What type of growth is involved in this process?

A
  • mesenchyme is directly ossified by osteoblasts, there is no cartilage anlagen
  • Appositional growth: direct deposit of new bone on pre-existing surface
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21
Q

What are the different zones seen in an active growth plate with ongoing endochondral ossification?

A

reserve zone, proliferation, hypertrophy, mineralization, and primary spongiosa

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22
Q

Where does remodeling of bone take place? What does it consist of? What is it regulated by?

A
  • within the bone (or basic) multicellular unit (BMU)
  • consists of a unit of coupled osteoblast and osteoclast activity on the bone surface
  • regulated by cell-cell interactions and cytokines
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23
Q

When is peak bone mass achieved?

A

Early adulthood after cessation of skeletal growth

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24
Q

At what point is bone resorption > formation?

A

-fourth decade

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25
Q

RANK

What is it?

Where is it expressed?

Function?

A

What is it: receptor activator for NF-kB

Where is it expressed = Osteoclast precursors

Function = Breakdown; when stimulated by RANKL, activates transcription factor NF-kB, which is essential for generation and survival of osteoclasts

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26
Q

RANK-L

Where is it expressed?

Function?

A

Where is it expressed = Osteoblasts and marrow stromal cells

Function = Breakdown

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27
Q

OPG

Where is it expressed?

Function?

A

Where is it expressed = “Decoy” receptor made by osteoblasts that can bind RANKL and prevent it’s interaction with RANK

Function = Build

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28
Q

What is the function of WNT/B-catenin?

A

WNT proteins (produced by osteoprogenitor cells) bind to LRP5 and LRP6 receptors on osteoblasts → thus trigger activation of B-catenin and production of OPG

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29
Q

A product produced by osteocyte inhibits the WNT/Beta-catenin pathway. What is it? What happens if the WNT/B-catenin pathway is blocked?

A
  • Sclerostin
  • if it is blocked then it suppresses bone formation
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30
Q

The balance between net bone formation and resorption is modulated by what two things?

A

-RANK

&

-WNT

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31
Q

What are the common building circulating hormones/factors?

A

Estrogen

Testosterone

Vit D

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32
Q

What are the common breakdown circulating hormones/factors?

A

PTH

IL-1

Glucocorticoids

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33
Q

What is M-CSF?

A

Macrophage colony stimulating factor

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34
Q

Function of M-CSF?

A

M-CSF receptor on osteoclast precursors STIMULATES tyrosine kinase cascade that is crucial for generation of osteoclasts

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35
Q

What type of cell signaling occurs between osteoclasts and osteoblasts? What occurs during this cell signaling?

A
  • Paracrine crosstalk between osteoblasts and osteoclasts
  • breakdown of matrix by osteoclasts liberates and activates matrix proteins, growth factors, cytokines, and enzymes; some of which stimulate osteoblasts
  • breakdown of bone to its elemental units which are released into the microenvironment stimulate its renewal
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36
Q

What are the (3) primary developmental disorders of bone?

A

Osteogenesis imperfecta

Osteopetrosis

Mucopolysaccharidoses

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37
Q

What is dysostosis and what is commonly associated with this?

A
  • localized disruption of migration and condensation of mesenchyme and differentiation into cartilage anlage
  • Transcription factor defects: specifically homeobox genes
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38
Q

What happens if there is a defect in homeobox proteins?

A

abnormal differentiation in osteoblasts and chondrocytes

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39
Q

Which gene is associated with Brachydactyly types D and E?

What is the disease manifestation?

A

HOXD13

-short terminal phalanges of thumb and big toe

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40
Q

Which gene mutation is associated with cleidocranial dysplasia?

A

RUNX2

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41
Q

What are the disease manifestations of cleidocranial dysplasia?

Inheritance pattern:

Presentation: six things

A

Inheritance pattern: AD

Presentation:

  • patent frontanelles
  • delayed closure of cranial sutures
  • Wormian bones
  • Delayed eruption of secondary teeth
  • Primitive clavicles
  • short height
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42
Q

Define:

Dysplasia

A

Global disorganization of bone &/or cartilage

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43
Q

Define:

Syndactyly/Craniosynostosis

A

Abnormal fusion of bones

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44
Q

What are wormian bones?

A

Extra bones within cranial sutures

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45
Q

What is an excellent way to determine the origin of a dwarfism pathology?

Can you give examples?

A

Look at the chest cavity!

Normal trunk length with achondroplasia

Small chest cavity with thanatophoric dysplasia

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46
Q

Achondroplasia

Gene mutation?

Presentation?

Mortality?

A

Gene mutation = Autosomal dominant FGFR3 gain of function

Presentation = Short extremities, normal trunk length, enlarged head, bluging forehead, depression root of nose

Mortality = NO change in longevity, intelligence or reproductive status

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47
Q

Thanatophoric dysplasia

Gene mutation?

Pathophysiology?

Presentation?

Mortality?

A

Gene mutation = FGFR3 gain of function (more severe phenotype)

Pathophysiology= diminished proliferation of chondrocytes and disorganization in the zone of proliferation

Presentation = Small chest cavity, bell-shaped abdomen, micromelic shortening of limbs, frontal bossing

Mortality = Die at birth or soon after

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48
Q

What is another name for osteogenesis imperfecta and what type of disease is this?

A
  • aka Brittle bone disease
  • deficiencies in type I collagen synthesis; most common inherited disorder of connective tissue
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49
Q

What causes osteogenesis imperfecta (OI)?

A

it is caused by mutations in genes encoding the alpha1 and alpha2 chains of type 1 collagen → mutated collagen peptides and no triple helix formation

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50
Q

Osteogenesis imperfecta:

Which type has the best prognosis?

Worst?

A

Best = Type I

Worst = Type 2

  • mutant collagen is associated with severe or lethal forms
  • decreased synthesis of normal collagen = mild skeletal abnormalities
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51
Q

What are the features of Type II OI?

A
  • there is no triple helix, it is uniformly fatal in utero, there is extraordinary bone fragility with multiple intrauterine fractures
  • the collagen is improperly formed
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52
Q

What are the features of Type I OI?

A
  • normal life span, childhood fractures that decrease in frequency following puberty
  • the collagen structure is normal, but the amount is < normal
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53
Q

Prognosis of Type II osteogenesis imperfecta?

A

Uniformly fatal in utero

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54
Q

Buzz word association for osteogenesis imperfecta type 2?

A

“Accordion-like” shortening of the limbs

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55
Q

What is the collagen defect associated with type I OI?

A

COL1A1

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56
Q

What is the collagen defect associated with Type II OI?

A

COL1A1 or COL1A2

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57
Q

What is the most severe subtype of OI in babies who do not die as newborns?

A

type III

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58
Q

What are the major clinical features of osteogenesis imperfecta?

A

Blue sclera

Skeletal fragility

Dentinogenesis imperfecta (small teeth)

Hearing impairment

Joint laxity

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59
Q

What is the most common type of osteogenesis imperfecta?

A

Type I

Also the mildest type of OI

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60
Q

Why is type II typically fatal?

A

Respiratory problems

(They have underdeveloped lungs from small thoracic cage)

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61
Q

What is the difference in sclera appearance b/w Type III and Type IV OI?

A

Type III = Blue, purple or gray tint

Type IV= White

*Remember; The order of best prognosis to worst is (1–> 4 –>3–>2) because fuck, lets make this difficult. But yeah, remember that type 4 is less severe, so the sclera are going to be normal in color.

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62
Q

What is the treatment of OI?

A
  • surgical rodding of long bones
  • exercise, keep a healthy weight, good nutrition
  • don’t smoke, don’t take steroids
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63
Q

What types of fractures are typically observed in both child abuse and OI?

A
  • fractures in multiple stages of healing
  • rib fractures
  • spiral fractures
  • fractures for which there is no adequate explanation of trauma
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64
Q

What is the best way to tell the difference between OI and child abuse?

A

bone pathology

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65
Q

Osteopetrosis

Aka?

A

Marble bone disease

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66
Q

What is the pathophysiology of osteopetrosis aka marble bone disease?

A

decreased bone resorption due to deficient osteoclast development/function → diffuse, symmetric skeletal sclerosis

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67
Q

What is Albers-Schonberg disease?

gene mutation?

What does it code for?

A

a mild autosomal dominant form of osteopetrosis

  • gene mutation= CLCN7
  • encodes a proton-chloride exchanger on the osteoclast surface that is required for resorption pit acidification
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68
Q

What is the cause of most cases of autosomal recessive osteopetrosis?

What does this encode?

A

a mutation of TCIRG1

-encodes a subunit of the osteoclast vacuolar H+-ATPase that is also necessary for acidification of the resorption pit

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69
Q

What is the deficiency in other causes of autosomal recessive osteopetrosis?

A

Carbonic anhydrase 2 (CA2)

70
Q

What is the function of carbonic anhydrase 2 (CA2)?

-What is often associated with deficiency of CA2?

A

it is required by osteoclast and renal tubular cells to generate protons from carbon dioxide and water

-renal tubular acidosis

71
Q

What are the features of osteopetrosis?

A

bones lack a medullary cavity, bulbous ends of long bones, neural foramina are small and compress nerves

-deposited bone is not remodeled and tends to be woven rather than lamellar

72
Q

How does osteopetrosis appear on Xray?

Buzz word association?

A

Erlenmeyer flask

73
Q

Inheritance pattern for osteopetrosis-severe infantile type?

Populations?

A

Autosomal recessive

Mediterranean and Arab race

74
Q

Common clinical features of osteopetrosis- severe infantile type?

A
  • Postpartum mortality: fractures, anemia, and hydrocephaly; repeated (fatal) infection due to leukopenia
  • extramedullary hematopoiesis leads to hepatosplenomegaly

Cranial nerve deficits:

Optic atrophy, deafness, facial paralysis

75
Q

What are the features of the autosomal dominant form of osteopetrosis?

A
  • mild
  • diagnosed in adolescence or adulthood
76
Q

How can osteopetrosis be treated?

A

hematopoietic stem cell transplantation

77
Q

What is seen on histology with osteopetrosis?

A

No medullary cavity

78
Q

What type of disease is mucopolysaccharidoses?

A

Lysosomal storage disease

79
Q

What is mucopolysaccharidoses?

  • What enzymes are mostly affected?
  • Where do mucopolysaccharides accumulate?
A
  • deficiency in enzymes that degrade dermatan sulfate, heparan sulfate, and keratan sulfate
  • Mostly acid hydrolase enzymes affected
  • mucopolysaccharides accumulate in the chondrocytes
80
Q

What is the result of extracellular mucopolysaccharide accumulation?

A

structural defects in articular cartilage

81
Q

what are the clinical manifestations of mucopolysaccharidoses?

A

short stature, chest wall abnormalities, and malformed bones

82
Q

What are examples of acquired bone disorders (5)?

A

Osteopenia/osteoporosis

Pagets

Osteomalacia/rickets

Hyperparathyroidism

Renal osteodystrophy

83
Q

What are 3 primary causes of osteoporosis?

A
  1. idiopathic
  2. postmenopausal
  3. senile
84
Q

Define osteopenia

Define osteoporosis

A

Osteopenia = decreased bone mass: 1.0 - 2.5 standard deviations below the mean

Osteoporosis = Osteopenia severe enough to increase risk of fracture. Bone mass at least 2.5 SD below the mean peak bone mass in young adults

85
Q

If your patient has a bone mass that is less than 2.5 SD below the mean, but you still diagnose them with osteoporosis, what MUST have happened? aka what signifies osteoporosis?

A

Atraumatic

or

Vertebral compression fractures

86
Q

What are the most common forms of osteoporosis?

A

senile and postmenopausal

87
Q

the magnitude of deficits in bone formation that accrues with every resorption and formation cycle is determined largely through what?

A

magnitude determined largely through hereditary factors

88
Q

Normal age-related bone loss average is what?

A
  1. 7% per year
    - equal loss between sexes
    - more rapid in caucasians than those of African descent
89
Q

How is senile osteoporosis classified?

What are the features of senile osteoporosis?

A
  • senile osteoporosis is classified as a low turnover variant
  • age-related changes include a reduced proliferative and biosynthetic potential (decreased capacity to make bone)
  • decreased cellular response to growth factors
90
Q

How does physical activity affect the rate of osteoporosis?

A

decreased physical activity leads to an increased rate of bone loss

-mechanical forces stimulate an increase in normal bone remodeling

91
Q

When considering physical activity, which exercise is better in the prevention against osteoporosis? Why?

A
  • resistance exercises are better
  • the effect of load magnitude on bone density is greater than load repetition
92
Q

What genetic factors could contribute to osteoporosis?

A
  • LRP5 single gene defect (rare)
  • polymorphisms in certain genes may contribute to variation in peak bone density within populations (most common are: RANKL, OPG, RANK, HLA locus, estrogen receptor gene, vit D receptor gene)
93
Q

What population is at risk of never obtaining their full potential bone mass due to eating disorders?

A

Adolescent girls

(Insufficienct calcium intake during period of rapid growth restricts their peak bone mass)

94
Q

How do calcium, PTH, and vitamin D contribute to the pathogenesis of senile osteoporosis?

A

calcium deficiency, increased PTH, and decreased vitamin D all contribute to senile osteoporosis

95
Q

What is a major hormonal influence on osteoporosis?

A

Menopause

(estrogen deficiency)

96
Q

How does decreased estrogen lead to osteoporosis and what variant is estrogen deficiency classified as?

A

decreased estrogen leads to an increase in both resorption and formation, but formation < resorption

  • high turnover variant
  • decreased estrogen leads to an increase in inflammatory cytokines (IL-6, TNF, and IL-1) → increased RANKL and decreased OPG → increased osteoclast recruitment and activity
97
Q

Chemotherapy for what cancer has an association with an increased risk of developing osteoporosis?

A

standard therapies for breast cancer (Tamoxifen) can increase bone loss

98
Q

What is the histological hallmark of osteoporosis?

A

normal bone, decreased in quantity

99
Q

Which types of bones are likely to be affected by postmenopausal osteoporosis?

How does postmenopausal osteoporosis affect these bones?

A
  • bones with increased surface area (cancellous bones of vertebral bodies)
  • the trabecular plates become perforated and thinned and lose their interconnections leading to microfractures and vertebral collapse
100
Q

How does senile osteoporosis affect bones?

A

the cortex becomes thinned by subperiosteal and endosteal resorption, and the Haversian systems are widened

101
Q

Describe the appearance of osteoporotic bone

A

(Right)

Loss of horizontal trabeculae and thickened vertical trabeculae

102
Q

What is the clinical course of osteoporosis?

A
  • vertebral fractures: thoracic and lumbar
  • loss of height
  • fractures of femoral neck, pelvis, or spine → immobilization
103
Q

What spinal changes are associated with loss of height in osteoporosis?

A

Lumbar lordosis & kyphoscoliosis

104
Q

What are 3 methods of prevention used against osteoporosis?

A

exercise, calcium, and vitamin D

105
Q

What are 4 methods of treatment for osteoporosis?

A
  • bisphosphonates (decrease osteoclast activity and induce apoptosis)
  • hormone therapy
  • Denosumab (anti-RANKL) (tx for postmenopausal osteo)
  • Anti-sclerostin and Cathepsin K inhibitors (investigational)
106
Q

What is the method of diagnosis for osteoporosis?

A

DEXA-scan

-early signs may not even show up on an x-ray (need more than 30% bone loss to detect on plain film)

107
Q

Why are blood tests used when diagnosing osteoporosis?

A

to check for secondary causes of osteoporosis, such as renal or hepatic failure, hyperthyroidism

108
Q

Risk factors for osteoporosis?

A

Caucasian, light colored eyes and skin

Nutrition (too much phosphorus-soda)

Smokers

109
Q

What do rickets and osteomalacia have in common in regards to their pathogenesis?

A

both are manifestations of vitamin D deficiency or its abnormal metabolism

-there is impairment of mineralization leading to accumulation of unmineralized matrix

110
Q

What is the main difference between osteoporosis and rickets/osteomalacia?

A
  • with osteoporosis the mineralization of bone is normal, the bone mass is just decreased
  • with rickets/osteomalacia, there is an impairment of mineralization and resultant accumulation of unmineralized matrix
111
Q

What is rickets?

A

rickets refers to the disorder in children, in whom it interferes with the deposition of bone in the growth plates

112
Q

What is osteomalacia?

A

the adult counterpart, in which bone formed during remodeling is undermineralized and predisposed to fractures

113
Q

What are 4 other causes of rickets?

A

renal rickets, hypophosphatemia, malabsorption, short-gut syndrome

114
Q

What is the clinical manifestation of rickets?

A

frontal bossing

squared off head

rachitic rosary of ribs

anterior protrusion of chest, pigeon breast deformity

lumbar lordosis

bowed legs

115
Q

What is the function of PTH?

A

calcium homeostasis →net result of PTH = increased serum calcium

116
Q

What effect does PTH have on calcium homeostasis? (4 things)

A
  • osteoclast activation (increased bone resorption and Ca2+ mobilization. PTH mediates the effect indirectly by increasing RANKL expression on osteoblasts)
  • increased resorption of Ca2+ by renal tubules
  • increased urinary excretion of phosphates
  • increased synthesis of active vitamin D by the kidneys
117
Q

What are the two types of hyperparathyroidism and what are their causes?

A
  • primary: autonomous parathyroid secretion
  • secondary: underlying renal disease (usually less severe than primary)
118
Q

Elevated PTH is responsible for bone changes in primary hyperparathyroidism, but additional factors contribute in secondary hyperparathyroidism. What are these factors?

A

chronic renal insufficiency

hyperphosphatemia

metabolic acidosis and aluminum deposition

119
Q

Hyperparathyroidism leads to significant skeletal changes related to _____ _______ _______

-this leads to what?

A

unabated osteoclast activity

-leading to increased bone fractures, bone deformities, and joint problems

120
Q

What are the 3 skeletal abnormalities seen with untreated primary hyperparathyroidism?

A
  • osteoporosis
  • brown tumors
  • osteitis fibrosa cystica
121
Q

How does osteoporosis present in cases of hyperparathyroidism?

A
  • most severe in the phalanges, vertebrae, and proximal femur
  • there is increased osteoclast activity most prominent in cortical bone, medullary bone not spared
122
Q

What is dissection osteitis?

What disease is it associated with?

A
  • when clasts tunnel into and dissect centrally along the length of trabeculae, adjacent marrow spaces are replaced by fibrovascular tissue
  • gives the appearance of railroad tracks
  • associated with hyperparathyroidism
123
Q

What is the histology associated with hyperparathyroidism?

A

Train tracks

124
Q

what is a brown tumor?

A

bone loss predisposes to microfractures, secondary hemorrhage, macrophage recruitment, and ingrowth of reparative fibrous tissue → mass lesion

125
Q

what makes brown tumors brown?

A

vascular, hemorrhage, and hemosiderin deposition; can undergo cystic degeneration

126
Q

What is von Recklinghausen disease of bone?

What disease is it associated with?

A
  • the combination of increased bone cell activity, peritrabecular fibrosis, and cystic brown tumors
  • hallmark of severe hyperparathyroidism
  • aka generalized osteitis fibrosis cystica
127
Q

What is renal osteodystrophy?

A

-skeletal changes that occur in chronic renal disease, including those associated with dialysis

128
Q

what are 3 different histologic bone changes associated with renal osteodystrophy?

A
  • high-turnover osteodystrophy: increased bone resorption and bone formation; resorption > formation
  • low-turnover or aplastic disease: adynamic bone (little osteoclastic and blastic activity) and less commonly osteomalacia
  • mixed pattern of disease: areas with high turnover and low turnover
129
Q

Kidney disease causes skeletal abnormalities through 3 mechanisms- what are these mechanisms?

A
  1. tubular dysfunction
  2. secondary hyperparathyroidism
  3. decreased biosynthetic function: decreased vitamin D hydroxylation
130
Q

What is occurring in tubular dysfunction that leads to renal osteodystrophy?

A

renal tubular acidosis, associated systemic acidosis dissolves hydroxyapatite → matrix demineralization and osteomalacia

131
Q

what is occurring in secondary hyperparathyroidism to lead to renal osteodystrophy?

A

there is a decrease in phosphate excretion, chronic hyperphosphatemia, and hypocalcemia

132
Q

Which population is renal osteodystrophy most serious?

A

children- because their bones are still growing

133
Q

What are 2 consequences of renal osteodystrophy occurring in children?

A
  • renal rickets: when the legs bend inward or outward
  • short stature
134
Q

Paget disease aka?

What is occurring in this disease?

A

Osteitis deformans

-increased but disordered and structurally unsound bone mass

135
Q

Paget disease

Characteristsics?

Gene?

A

Polyostotic (involves multiple bones) (85% of cases)

70yo average age

Caucasians

SQSTM1 gene

136
Q

What is the pathogenesis of Paget Disease?

A

uncertain, but both genetic and environmental contributions

50% familial and 10% of sporadic cases are associated with mutations in the SQSTM1 gene

137
Q

what happens when the SQSTM1 gene is mutated?

A

there is increased activity of NF-kB leading to increased osteoclast activity

138
Q

Paget disease

Buzz word association with Xray appearance?

A

“Cotton Wool”

139
Q

What is the paget disease hallmark morphology?

A

Mosaic pattern of lamellar bone seen in sclerotic phase

Jigsaw-like appearance with prominent cement lines

140
Q

what are the 3 stages of Paget?

A
  1. initial osteolytic stage
  2. mixed osteoclastic-osteoblastic phase
  3. burned-out quiescent osteosclerotic stage
141
Q

what are the characteristic features associated with the initial osteolytic stage?

A

large osteoclasts with 100 nuclei

142
Q

what are the characteristic features associated with mixed osteoclastic-osteoblastic phase?

A

clasts persist, but lots of blasts also; primarily osteoblastic at end of stage

143
Q

what are the characteristic features associated with burned-out quiescent osteosclerotic stage?

A

osteoblast activity predominates

-coarsely thickened trabeculae and cortices that are soft and porous, lacking structural stability; fractures easily

144
Q

What is the most dreaded complication of Paget disease?

A

sarcomatous transformation

-seen in less than 1% of cases, often osteosarcoma or fibrosarcoma in long bones, pelvis, skull, and spine

145
Q

What type of fractures are associated with paget disease?

A

-Chalk stick type fractures in the long bones of legs

-Compression fractures of spine → spinal cord injury and kyphosis

146
Q

What are the lab values associated with paget disease?

A

Elevated serum ALK PHOSPHATASE

NORMAL = Calcium and phosphorous

147
Q

Name a unique clinical feature of paget disease

A

Hypervascularity of paget disease

Warms the overlying skin

→ Can lead to high output heart failure

148
Q

What is the treatment for Paget disease?

A

calcitonin and bisphosphonates to suppress symptoms

149
Q

Define:

Simple fracture

A

Overlying skin intact

150
Q

Define:

Compound fracture

A

Bone communicates with the skin surface

151
Q

Define:

Comminuted fracture

A

Bone is fragmented

152
Q

Define:

Displaced fracture

A

Ends of the bone at the fracture site are not aligned

153
Q

Define:

Stress fracture

A

Slowly developing fracture that follows a period of increased physical activity in which bone is subjected to repetitive loads

nice.

154
Q

Define:

Greenstick fracture

A

Extending only partially through the bone, common in infants when bones are soft

155
Q

Define:

Pathologic fracture

A

Involving bone weakened by an underlying disease process such as a tumor

156
Q

What is osteonecrosis?

A

Infarction of the bone and marrow

(pretty common)

157
Q

What causes most cases of osteonecrosis?

A

Fractures

or

Corticosteroid tx (iatrogenic)

158
Q

How do subchondral infarcts present?

What is the morphology of subchondral infarcts?

A

they cause pain initially associated only with activity then becomes constant

  • subchondral infarcts often collapse and may lead to severe secondary osteoarthritis
  • they are triangular or wedge-shaped with the subchondral bone plate as its base → necrosis
159
Q

How do medullary infarcts typically present?

A

they are usually small and clinically silent

160
Q

What region is typically not affected in osteonecrosis?

Why?

A

Cortex is not affected

Due to collateral flow

161
Q

Buzz word association with osteonecrosis?

A

“Creeping substitution”

162
Q

What is osteomyelitis?

A

Inflammation of the bone and marrow

Typically following infection

163
Q

What are most cases of osteomyelitis caused by?

A

Pyogenic bacteria

&

Mycobacteria

164
Q

How does pyogenic osteomyelitis typically spread in:

Kids?

Adults?

A

Kids = Hematogenous

Adults = Complication of open fractures, surgical procedures and diabetic infections

165
Q

Most common cause of pyogenic osteomyelitis?

A

Staph aureus (80-90%)

166
Q

Osteomyelitis:

Name the associated organism with:

Sickle cell patients

A

Salmonella

167
Q

Osteomyelitis:

Name the associated organism with:

MAC deficiency

168
Q

What is:

Sequestrum?

Involucrum?

A

Sequestrum = Dead bone following abscess

Involucrum = New bone

169
Q

What is the histology associated with mycobacterial osteomyelitis?

A

Caseous necrosis and granulomas

170
Q

What is Pott disease?

A

Aka Tuberculous spondylitis

Permanent compression fractures

171
Q

What are the associated bone deformities seen with skeletal syphilis?

A

Saber shin

Saddle nose

172
Q

what are the characteristic features associated with burned-out quiescent osteosclerotic stage?

A

osteoblast activity predominates

-coarsely thickened trabeculae and cortices that are soft and porous, lacking structural stability; fractures easily

NMSP Exam II (17 decks)

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